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C a r d i a = gastr-esoph. junction, the junctional zone between pale squamous esophageal mucosa and pink gastric mucosa, Z line . Up to 3 cm. of gastric mucosa type extending up the esophagus is accepted as normal More than that indicates Barrets esophagus Assessment of Diseases of the oesophagus:
Careful history Physical examination Appropriate investigation Symptoms :
Dysphagia: difficulty in swallowing Dysphagia-May be due to- organic disease (benign strictures or esophageal carcinoma) esophagal motility disorders (achalasia or diffuse esophageal spasm)
Dysphagia for solids implies severe disease, organic or functional
Dysphagia for liquids indicates motility disordersor motility Regurgitation means effortless return of gastric content into the mouth
Postural regurgitation is a common symptom in reflux disease
Precipitated by meals and increased in intraabdo.pressure
Overflow regurgitation into the pharynx-trachea leads to aspiration pneumonitis
Odynophagia means painful swallowing- organic disease e.g. esophagitis
Esophageal painare of two sorts: heartburn and angina-like tightening pain
Heartburn is due to reflux of gastric juice to the esophagus- esophagitis
Angina-like tightening pain-esophageal anterior chest pain, simulates angina pectoris- reflux esophagitis, motility disorders
Atypical symptoms :
Anemia due to chronic blood loss- erosive esophagitis
Acute upper GI bleeding- Mallory-Weiss sdr.,peptic ulcer in a hiatus herniaulcer in a
Severe sepsis, respiratory distress- perforation of the esophagus
Angina-like pain- reflux disease associated with nocte coughing
Pulmonary symptoms- aspiration pneumonitis- reflux disease
Signs Inaccesible to physical examination
Evidence of weight loss
Palor due anemia
Neck swelling due to diverticulum
Chest signs
Hepatomegaly
Investigations:
CXR, Barium swallow, CT scan USS, external, endoscopic( EUS )
Radioisotope studies- labelled bollus Endoscopy with biopsy, cytology Manometry Ph 24-hours monitoring
Tests to exclude cardiac disease- ECG coronary angiography
CT scan- preop.assessment of esophageal malignancy
- extent of mural invasion,
- involvement of adjacent structures,
- mediastinal lymph nodesmotility disorders
ESOPHAGEAL MOTILITY DISORDERS
1 . Cricopharyngeal dysfunction
2 . Achalasia
3 . Diffuse esophgeal spasm
Cricopharyngeal dysfunction :
Failure of the UES to relax properly leads to Pharyngoesofageal diverticulum- Zenkers
False diverticulum- mucosa herniates posteriorly between the fiber of CPH.muscle
Frequently associated with hiatus hernia and GERD.
Symptoms: dysphagia, mass in the neck, tracheal compression
Formation of pharyngoesophageal (Zenker's) diverticulum : Left- herniation of the pharyngeal mucosa and submucosa occurs at the point of transition between the oblique fibers of the thyropharyngeus muscle and more horizontal muscle and more horizontal fibers of the cricopharyngeus muscle (Killian's triangle).
Achalasia :Unknown etiology Abnormal peristalsis in the body of the esophag resulting in: high resting LES pressure failure of the LES to relax during swallowing . The body of the esophagus becomes dilated. Carcinoma of the esophagus is 10 times commoner in pts. with achalasia . Symptoms : Difficulty in swallowing fluids Respiratory symptoms Vomiting Retrosternal pain Weight loss
Pathogenesis of Achalasia ( Read this in Davidson's Textbook )
Diagnosis:
1 . Ba contrast studies- smooth tapering narrowing of lower esoph. end . with dilated, tortuous lower esophagus, uncoordinated or absent peristalsis ( Bird Be3ak appearance on Ba swallow )peristalsis
2 .Esophageal manometry
3 . Esophagoscopy
Treatment of Achalasia
1 . Non surgical treatment- pneumatic dilatation of the LES
2 . Surgical- esophagomyotomy (Hellers op.)
Myotomy is confined to the lower portion of the esophagus, 7-10 cm. and upper gastric muscle
Esophagomyotomy can be combined with an antireflux procedure
As the degenerative neural lesion of this disease cannot be corrected, treatment is directed at palliation of symptoms and prevention of complications.
Effective peristalsis is rarely restored by successful treatment, but improved oesophageal emptying and a decrease in oesophageal diameter are generally expected.
3 . Pharmacotherapy Smooth muscle relaxants alleviate symptoms and improve oesophageal emptying in up to 70% of patients. Nitrites, such as sublingual isosorbide dinitrite, and calcium channel blockers such as diltiazem, nifedipine and verapamil, have this effect. This treatment option is suitable for patients with medical conditions that interfere with dilatation or myotomy.
Botulinum toxin type A is derived from the controlled fermentation of Clostridium botulinum. The toxin binds to presynaptic cholinergic neuronal receptors, interferes with acetylcholine release.
Botulinum toxin decreases LOS basal tone and improves
symptoms in patients with achalasia. Beneficial response occurs in 90% of patients, but symptoms reappear within a year in many initial responders.
Dilatation :Forceful dilatation of the gastroesophageal sphincter to a diameter of 3 cm is necessary to tear the circular muscle and to ensure a lasting reduction in LOS pressure.
Pneumatic dilators are conventionally used today.
Water-soluble contrast material is used to detect distal oesophageal leaks.
Surgical consultation is undertaken if perforation is evident.
Small perforations are managed conservatively with broad-
spectrum antibiotics.
Clinical deterioration e.g. shock, sepsis, haemorrhage or a
finding of free-flowing barium into the mediastinum, requires
immediate thoracotomy and repair. The response rate varies with patient age, (younger patients do not do as well as older patients), and duration of symptoms, (those with a shorter history do not respond as well)
Morbidity is mostly related to oesophageal perforation a complication in approximately 5% of patients, but surgical repair is required in less than half of these cases.
The Heller procedure was described in 1913 and now a modification of this procedure is used most commonly in the surgical management of achalasia . An anterior myotomy is performed by dividing the circular muscle of the oesophagus down to the level of the mucosa.
A preferable alternative to open myotomy, allowing the Heller myotomy to be performed thoracoscopically and laparoscopically The Benefits include Shorter hospitalisation, less pain and early resumption of activity are the benefits of the minimally invasive approach, which remains as effective as the open techniques in the relief of dysphagia. Complications of minimally invasive surgery include: anterior gastric perforation, mucosal perforation at the gastroesophagea (GO) junction and, most significantly, GOR
Comparisons between therapies : Pneumatic dilatation, pharmacotherapy and botulinum toxin injection are easy to use, usually well-tolerated and relatively cheap treatment options in achalasia. Surgery generally gives longer-lasting results as well as more complete relief of symptoms. h n ~ ðmV; 5h{ 5B*CJ OJ PJ QJ \^J aJ mH ph sH -h{ h
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